Severe Uncompensated Metabolic Alkalosis due to Plasma Exchange in a Patient with Pulmonary-Renal Syndrome: A Clinician’s Challenge
Metabolic alkalosis secondary to citrate toxicity from plasma exchange is very uncommon in patients with normal renal function. In patients with advanced renal disease this can be a fatal event. We describe a case of middle-aged woman with Goodpasture’s syndrome treated with plasma exchange who deve...
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Wiley
2015-01-01
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| Series: | Case Reports in Critical Care |
| Online Access: | http://dx.doi.org/10.1155/2015/802186 |
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| author | Mohsin Ijaz Naeem Abbas Dmitry Lvovsky |
| author_facet | Mohsin Ijaz Naeem Abbas Dmitry Lvovsky |
| author_sort | Mohsin Ijaz |
| collection | DOAJ |
| description | Metabolic alkalosis secondary to citrate toxicity from plasma exchange is very uncommon in patients with normal renal function. In patients with advanced renal disease this can be a fatal event. We describe a case of middle-aged woman with Goodpasture’s syndrome treated with plasma exchange who developed severe metabolic alkalosis. High citrate load in plasma exchange fluid is the underlying etiology. Citrate metabolism generates bicarbonate and once its level exceeds the excretory capacity of kidneys, the severe metabolic alkalosis ensues. Our patient presented with generalized weakness, fever, and oliguria and developed rapidly progressive renal failure. Patient had positive serology for antineutrophilic cytoplasmic antibodies myeloperoxidase (ANCA-MPO) and anti-glomerular basement membrane antibodies (anti-GBM). Renal biopsy showed diffuse necrotizing and crescentic glomerulonephritis with linear glomerular basement membrane staining. Patient did not respond to intravenous steroids. Plasma exchange was started with fresh frozen plasma but patient developed severe metabolic alkalosis. This metabolic alkalosis normalized with cessation of plasma exchange and initiation of low bicarbonate hemodialysis. ANCA-MPO and anti-GBM antibodies levels normalized within 2 weeks and remained undetectable at 3 months. Patient still required maintenance hemodialysis. |
| format | Article |
| id | doaj-art-356a4e4514824f26bb4190ecbf44f109 |
| institution | OA Journals |
| issn | 2090-6420 2090-6439 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Case Reports in Critical Care |
| spelling | doaj-art-356a4e4514824f26bb4190ecbf44f1092025-08-20T02:24:08ZengWileyCase Reports in Critical Care2090-64202090-64392015-01-01201510.1155/2015/802186802186Severe Uncompensated Metabolic Alkalosis due to Plasma Exchange in a Patient with Pulmonary-Renal Syndrome: A Clinician’s ChallengeMohsin Ijaz0Naeem Abbas1Dmitry Lvovsky2Division of Pulmonary and Critical Care Medicine, Department of Medicine, Bronx Lebanon Hospital Center, 1650 Selwyn Avenue, Suite 12F, Bronx, NY 10457, USADepartment of Medicine, Bronx Lebanon Hospital Center, 1650 Selwyn Avenue, Suite 10C, Bronx, NY 10457, USADivision of Pulmonary and Critical Care Medicine, Department of Medicine, Bronx Lebanon Hospital Center, 1650 Selwyn Avenue, Suite 12F, Bronx, NY 10457, USAMetabolic alkalosis secondary to citrate toxicity from plasma exchange is very uncommon in patients with normal renal function. In patients with advanced renal disease this can be a fatal event. We describe a case of middle-aged woman with Goodpasture’s syndrome treated with plasma exchange who developed severe metabolic alkalosis. High citrate load in plasma exchange fluid is the underlying etiology. Citrate metabolism generates bicarbonate and once its level exceeds the excretory capacity of kidneys, the severe metabolic alkalosis ensues. Our patient presented with generalized weakness, fever, and oliguria and developed rapidly progressive renal failure. Patient had positive serology for antineutrophilic cytoplasmic antibodies myeloperoxidase (ANCA-MPO) and anti-glomerular basement membrane antibodies (anti-GBM). Renal biopsy showed diffuse necrotizing and crescentic glomerulonephritis with linear glomerular basement membrane staining. Patient did not respond to intravenous steroids. Plasma exchange was started with fresh frozen plasma but patient developed severe metabolic alkalosis. This metabolic alkalosis normalized with cessation of plasma exchange and initiation of low bicarbonate hemodialysis. ANCA-MPO and anti-GBM antibodies levels normalized within 2 weeks and remained undetectable at 3 months. Patient still required maintenance hemodialysis.http://dx.doi.org/10.1155/2015/802186 |
| spellingShingle | Mohsin Ijaz Naeem Abbas Dmitry Lvovsky Severe Uncompensated Metabolic Alkalosis due to Plasma Exchange in a Patient with Pulmonary-Renal Syndrome: A Clinician’s Challenge Case Reports in Critical Care |
| title | Severe Uncompensated Metabolic Alkalosis due to Plasma Exchange in a Patient with Pulmonary-Renal Syndrome: A Clinician’s Challenge |
| title_full | Severe Uncompensated Metabolic Alkalosis due to Plasma Exchange in a Patient with Pulmonary-Renal Syndrome: A Clinician’s Challenge |
| title_fullStr | Severe Uncompensated Metabolic Alkalosis due to Plasma Exchange in a Patient with Pulmonary-Renal Syndrome: A Clinician’s Challenge |
| title_full_unstemmed | Severe Uncompensated Metabolic Alkalosis due to Plasma Exchange in a Patient with Pulmonary-Renal Syndrome: A Clinician’s Challenge |
| title_short | Severe Uncompensated Metabolic Alkalosis due to Plasma Exchange in a Patient with Pulmonary-Renal Syndrome: A Clinician’s Challenge |
| title_sort | severe uncompensated metabolic alkalosis due to plasma exchange in a patient with pulmonary renal syndrome a clinician s challenge |
| url | http://dx.doi.org/10.1155/2015/802186 |
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